Ozone pollution is associated with increased rates of hospitalization for lung ailments like asthma attacks and for heart problems like heart attacks. Exactly how the pollutant -- a major component of smog, which is formed when smokestack and tailpipe emissions cook in the hot summer sun -- does its damage has been unclear.
New research at Duke University Medical Center suggests that ozone attacks the immune system, making those who breathe in the pollutant more susceptible to secondary infections.
At least, that's what happens to mice in the lab, according to new peer-reviewed research published today in the Journal of Immunology.
Exposure to ozone led not only to an increase in lung injury from bacterial toxins, but also a die-off of immune system cells designed to attack foreign invaders and keep airways clear.
"Small amounts of inhaled foreign material can be relatively harmless, since they stimulate an appropriate innate immune response that protects the lungs," Dr. John Hollingsworth, a pulmonologist and lead author of study, said in a statement made available to the press. "However, it appears that ozone causes the innate immune system to overreact, killing key immune system cells, and possibly making the lung more susceptible to subsequent invaders, such as bacteria."
Here's how the researchers described their study and some of its results:
The innate immune system is the most primitive aspect of the bodys defenses. Its cells react indiscriminately to any invader. One of the key cells in the innate immune system is known as a macrophage, Greek for "big eater."
For their experiments, the researchers had mice breathe either room air or air with levels of ozone meant to mirror what an exercising human would experience on a high, or unhealthy, ozone level day. After exposing all mice to the active portion of E. coli bacteria in aerosol form, the researchers studied how the innate immune system responded.
In the mice exposed to ozone, the airways of the lungs were hyperactive and we found higher concentrations of inflammatory cells, Hollingsworth said. But more significantly, ozone pre-exposure reduced the number of macrophages in the lung after secondary exposure to inhaled bacterial endotoxin. Exposure to ozone in this context had stimulated them to undergo programmed cell death, or apoptosis.
The researchers also found that the effect of the inhaled ozone was not limited to just the lungs. Mice exposed to ozone were also found to have lower levels of immune system cells circulating in the blood.
The Environmental Protection Agency has set a variety of new rules in recent years designed to limit the pollution that leads to ozone formation. It is also in the midst of setting a new limit for acceptable levels of ozone in the air.
Studies like this one suggest strict limits can have important health benefits.
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